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Changes in cellular glutathione levels: possible relation to selenium-mediated anticarcinogenesis

R A LeBoeuf, W G Hoekstra

    Federation Proceedings
    |June 1, 1985
    PubMed

    Insights

    Excess selenium (Se) intake reversibly inhibits mammalian cell proliferation, particularly in the G1 phase. This effect is linked to altered cellular glutathione levels, suggesting a role in anticarcinogenesis.

    Area of Science:

    • Biochemistry
    • Cell Biology
    • Toxicology

    Background:

    • Selenium (Se) is an essential trace element with known roles in antioxidant defense and cancer prevention.
    • Understanding the precise mechanisms by which Se influences cell growth is crucial for its therapeutic application.

    Purpose of the Study:

    • To investigate the mechanisms underlying Se-mediated anticarcinogenesis.
    • To determine the effects of excess Se on mammalian cell proliferation and cell cycle progression.
    • To explore the relationship between Se administration and cellular glutathione metabolism.

    Main Methods:

    • In vitro studies using mammalian cell cultures treated with excess sodium selenite (Na2SeO3).
    • Cell proliferation assays to assess growth inhibition.
    • Cell cycle analysis to identify affected phases (G1, S, G2).
    • Measurement of cellular glutathione concentrations in vitro and in vivo.

    Main Results:

    • Excess Se (as Na2SeO3) demonstrated a reversible inhibitory effect on mammalian cell proliferation in vitro.
    • The primary inhibitory effect was observed during the G1 phase of the cell cycle, with secondary effects on S and G2 phases.
    • Administration of excess Se altered cellular glutathione concentrations both in vitro and in vivo.

    Conclusions:

    • Excess Se intake can reversibly inhibit mammalian cell proliferation, impacting multiple cell cycle phases.
    • Altered cellular glutathione metabolism is a key factor in Se-mediated effects on cell proliferation.
    • These findings provide insights into the potential anticarcinogenic mechanisms of selenium.

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